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Published on: January 28, 2020
Fibrin clot properties in coronary artery disease: new determinants and prognostic markers
Julie B Larsen1, Anne-Mette Hvas2
1Thrombosis and Hemostasis Research Unit, Department of Clinical Biochemistry, Aarhus University Hospital, Aarhus, Denmark
Insights
Impaired fibrinolysis and altered clot properties significantly increase coronary artery disease (CAD) risk. Further research into modulating the fibrinolytic system could improve CAD treatment strategies.
Area of Science:
- Cardiovascular Medicine
- Hematology
- Thrombosis Research
Background:
- Coronary artery disease (CAD) remains a leading global cause of death, with traditional risk factors incompletely explaining its development.
- Platelets are known to play a role in atherosclerosis, but reduced fibrinolytic activity is increasingly recognized as a key factor in CAD progression.
Purpose of the Study:
- To review the regulators of fibrinolysis and factors influencing fibrin clot formation.
- To summarize biomarkers of altered fibrinolysis and current laboratory methods.
- To present evidence on fibrin clot properties in CAD patients and their significance for coronary thrombotic disease risk.
Main Methods:
- Literature review of fibrinolysis regulators and clot formation factors.
- Summary of fibrinolysis markers and laboratory techniques.
- Analysis of existing evidence comparing fibrin clot properties in CAD patients versus healthy individuals.
Main Results:
- Altered fibrin clot properties and impaired fibrinolysis are linked to increased thromboembolic risk in CAD patients.
- Biomarkers of fibrinolysis show potential as future CAD risk markers.
- Evidence suggests a significant contribution of fibrinolysis dysfunction to CAD pathophysiology.
Conclusions:
- Impaired fibrinolysis and abnormal fibrin clot structure are significant contributors to thromboembolic risk in coronary artery disease.
- Further investigation is needed to determine if targeting the fibrinolytic system can lead to improved CAD treatments.
- Biomarkers reflecting fibrinolytic activity warrant further study for their role in CAD risk assessment.
Abstract:
Despite improved diagnosis and treatment options, coronary artery disease (CAD) is still the leading cause of mortality and morbidity worldwide. Established risk factors such as smoking, hypercholesterolemia, and hypertension only partly explain the pathophysiology of CAD. Besides the well-known role of platelets in atherosclerosis and arterial thrombus formation, reduced endogenous fibrinolytic activity may play a key role in CAD formation and progression. Thus, biomarkers of fibrinolysis may be future CAD risk markers. In this review, we provide an overview of regulators of fibrinolysis and the main factors of importance to fibrin clot formation including coagulation factor XIII, thrombin, and fibrinogen. We summarize markers of altered fibrinolysis and current laboratory methods applied in clinical practice and research. We present today’s evidence on fibrin clot properties in patients with stable CAD or acute coronary syndrome compared with healthy individuals and the significance of altered fibrinolysis as a risk for coronary thrombotic disease. In conclusion, we found evidence that altered fibrin clot properties and impaired fibrinolysis appear to contribute significantly to the thromboembolic risk in CAD patients. Therefore, more research is crucial in order to clarify whether modulation of the fibrinolytic system may pave the way for improved treatment of CAD.
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